Treatment
Protecting the Heart
Current Treatment
All drugs currently used after myocardial infarction target neurohumoral pathways or platelet function, but no drug treats the underlying muscle damage.
This only acts to slow the progression of heart failure and somewhat reduce the likelihood of future major heart problems, resulting in a very poor long-term prognosis for MI.
Myocardial Infarction
Current Standard of Care
01.
Emergency Transfer
to Hospital
02.
Reperfusion by Percutaneous Coronary Intervention (PCI) “Stent”
03.
Long-term pharmacotherapy
+ Scarring & Failure
04.
Reduction in lifespan
and quality of life
Ischemia
Inadequate blood flow to the heart (ischemia), as occurs during heart disease, causes physiological stress to cardiac cells.
Stress lasting more than approx. 30 mins causes death of the cells and lasting damage whereas reversal of ischemia within this period preserves cellular function.
In the US the median time from MI symptoms to treatment (usually Percutaneous Coronary Intervention (PCI) or “stent”) is 185 mins, meaning most patients experience inevitable irreversible damage, with damage increasing in those patients with delayed time to PCI.
>30+
min ischemia
Cell death + lasting damage
0-30
min ischemia
No lasting damage
“It’s like growing old overnight…”
It is estimated that as much as 1.7% of the World’s population are living with Ischaemic heart disease, with a high risk of MI resulting in death or progression to heart failure; described by patients as
“It’s like growing old overnight, without gradual ageing giving you the chance to get used to it.”
The need for pharmacotherapy to add to the acute treatment of the heart after MI by cardiologists is clear. In the words of the European Society of Cardiology
“..still there is no therapy aimed at reducing (heart) injury that is clearly associated with improved clinical outcomes.”
Cardiac Function
Cardiac functional reserve is the difference between peak (i.e. maximal stress at peak exercise) and baseline resting values.
Cardiomyocyte death reduces normal heart fitness and lifespan after MI.
Cardiac functional reserve is the difference between peak (i.e. maximal stress at peak exercise) and baseline resting values. With increasing age, natural attrition results in progressive diminution in the pumping capability of the heart and cardiac reserve, while baseline resting cardiac function (dashed horizontal line) remains largely unchanged.
With discrete incidences of cardiomyocyte loss through myocardial infarctions pumping capability plummets stepwise with each incident. When this falls below the normal baseline level, a state of extreme cardiac failure (cardiogenic shock) ensues, which is rapidly followed by death unless drastic measures (e.g. surgery) are successful.
The accelerated deterioration of cardiac pumping capability (secondary to putative myocyte attrition) can be ameliorated with neurohumoral therapies.
(Adapted from Exp Physiol 2003 883. 447-458)
Learn More
Myocardial Infarction
Revolutionising Treatment After MI
01.
Emergency Transfer
to Hospital
02.
Forcefield Revolutionary Treatment + “Stent”
03.
Preserved Function
+ Reduced Scarring
04.
Extended Life
and Healthspan
Forcefield Therapeutics is pioneering proteins with the natural ability to retain heart function after myocardial infarction, by preserving cardiomyocytes, sustaining cardiac function and preventing clinical changes in the heart.
Forcefield has the potential to revolutionise acute post-myocardial infarction treatment which has previously seen decades of failure. We are adding to the toolbox that health professionals can use, improving outcomes and reducing the reliance on long term medication.
